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Inflammatory Response in the Hippocampus of PS1M146L/APP751SLMouse Model of Alzheimer's Disease: Age-Dependent Switch in the Microglial Phenotype from Alternative to Classic
Open accessAbstract
Although the microglial activation is concomitant to the Alzheimer's disease, its precise role (neuroprotection vs neurodegeneration) has not yet been resolved. Here, we show the existence of an age-dependent phenotypic change of microglial activation in the hippocampus of PS1xAPP model, from an alternative activation state with Aβ phagocytic capabilities (at 6 months) to a classic cytotoxic phenotype (expressing TNF-α and related factors) at 18 months of age. This switch was coincident with high levels of soluble Aβ oligomers and a significant pyramidal neurodegeneration.In vitro assays, using astromicroglial cultures, demonstrated that oligomeric Aβ42 and soluble extracts from 18-month-old PS1xAPP hippocampus produced a potent TNF-α induction whereas monomeric Aβ42 and soluble extract from 6- or 18-month-old control and 6-month-old PS1xAPP hippocampi produced no stimulation. This stimulatory effect was avoided by immunodepletion using 6E10 or A11. In conclusion, our results show evidence of a switch in the activated microglia phenotype from alternative, at the beginning of Aβ pathology, to a classical at advanced stage of the disease in this model. This change was induced, at least in part, by the age-dependent accumulation of extracellular soluble Aβ oligomers. Finally, these cytotoxic activated microglial cells could participate in the neuronal lost observed in AD.
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“Within the AD brain, there is a chronic activation of microglia associated with inflammatory cytokines including TNF␣ that can substantially block of ability of the microglia to remove 47,49,50 or degrade A. 51,52”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [49]
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“several studies have suggested that microglial activation plays a beneficial role in early stages of AD pathology, but contributes to disease worsening in late stages of AD [66–68].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [66]
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
Lesné, S., Koh, M. T., Kotilinek, L., Kayed, R., Glabe, C. G., Yang, A., Gallagher, M., & Ashe, K. H. (2006) · Nature · doi:10.1038/nature04533 · Cited by 2,769 · cited 2×
“The observed 6E10-positive bands corresponded with the reported Mr for the oligomeric A forms, detected by Western blots (see Lambert et al., 2007), and also similar to soluble oligomers identified in other aged tg models (Lesné et al., 2006).”
BackgroundRetractedAmyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Polazzi, E., Mengoni, I., Caprini, M., Peña‐Altamira, E., Kurtys, E., & Monti, B. (2012) · Neurosignals · doi:10.1159/000337115 · Cited by 9,023
Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis
Kayed, R., Head, E., Thompson, J. L., McIntire, T. M., Milton, S. C., Cotman, C. W., & Glabe, C. G. (2003) · Science · doi:10.1126/science.1079469 · Cited by 4,064 · cited 1×
“The soluble fractions (S1) were obtained by ultracentrifugation of the homogenates as described previously (Kayed et al., 2003).”
MethodWest, M. J., Slomianka, L., & Gundersen, H. J. G. (1991) · The Anatomical Record · doi:10.1002/ar.1092310411 · Cited by 2,994 · cited 2×
“The software calculated the estimated total number of cresyl-violet stained nuclei in the CA1 region using the optical fractionator formula (West et al., 1991; Schmitz and Hof, 2005), N 1/bsf.1/ssf.1/asf.1/hsf.”
MethodIL-17 family cytokines and the expanding diversity of effector T cell lineages
Weaver, C. T., Hatton, R. D., Mangan, P. R., & Harrington, L. E. (2007) · Annual Review of Immunology · doi:10.1146/annurev.immunol.25.022106.141557 · Cited by 1,842 · cited 1×
“The recruitment of CD4 Th1-cells in experimental autoimmune encephalomyelitis (EAE; a disease similar to human multiple sclerosis) induced the production of, among other cytotoxic factors, TNF- (Dhib-Jalbut et al., 2006; Weaver et al., 2007).”
BackgroundControl of microglial neurotoxicity by the fractalkine receptor
Cardona, A. E., Pioro, E. P., Sasse, M. E., Kostenko, V., Cardona, S. M., Dijkstra, I. M., Huang, D., Kidd, G., Dombrowski, S., Dutta, R., et al. (2006) · Nature Neuroscience · doi:10.1038/nn1715 · Cited by 1,531 · cited 1×
“…reported that aging and/or A could decrease the neuronal expression of microglial inhibitory factors, such as CD200, fractalkine or neurotransmitters (Acetylcholine or noradrenaline) (Cardona et al., 2006; Chitnis et al., 2007; Heneka and O’Banion, 2007; Lyons et al., 2007a; Duan et al., 2008).”
BackgroundThe efficiency of systematic sampling in stereology—reconsidered
GUNDERSEN, H. J. G., JENSEN, E. B. V., KIÊU, K., & NIELSEN, J. (1999) · Journal of Microscopy · doi:10.1046/j.1365-2818.1999.00457.x · Cited by 1,317 · cited 1×
“The precision of the individual estimations is expressed by the coefficient of error (CE) (Gundersen et al., 1999) and here we have estimated the total CE (CE group value) that was calculated using the CEs in each individual animal.”
MethodWyss-Coray (2006) · doi:10.1038/nm1484 · Cited by 1,284 · cited 1×
“As proposed by the inflammation hypothesis of Alzheimer’s disease (AD), the neurodegenerative process could be exacerbated by a chronic inflammatory response to -amyloid (A ) peptides (for review, see Griffin et al., 1998; Wyss-Coray, 2006; Heneka and O’Banion, 2007).”
BackgroundSimard, A. R., Soulet, D., Gowing, G., Julien, J.-P., & Rivest, S. (2006) · Neuron · doi:10.1016/j.neuron.2006.01.022 · Cited by 1,265 · cited 2×
“We observed a close spatial and temporal parallelism between A deposits and microglial activation (Simard et al., 2006).”
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Items 301–383 of 383
Peripheral Delivery of Neural Precursor Cells Ameliorates Parkinson’s Disease-Associated Pathology
Edwards, G. A., Gamez, N., Armijo, E., Kramm, C., Morales, R., Taylor-Presse, K., Schulz, P. E., Soto, C. A., & Moreno‐González, I. (2019) · Cells · doi:10.3390/cells8111359 · Cited by 10
“Glial burden was defined as the percentage of area stained with anti-GFAP (astrocytes), anti-BLBP (reactive astrocytes), anti-Iba1 (microglia) and anti-CD45 (macrophages) by the total area analyzed, as previously described [49,50].”
MethodCurcumin suppresses neuroinflammation to protect neurons by preventing NLRP3 inflammasome activation
Shi, Q., Zheng, Y., Wang, L., Xue, Y., & Yang, Y. (2021) · European Journal of Inflammation · doi:10.1177/20587392211058615 · Cited by 10
“It has been recently accepted that neuroinflammation is a characteristic factor involved in the pathological process of AD.23 Microglia are resident macrophages that participate in the immune regulation of the CNS. Aβ is generated by cleavage of the amyloid precursor protein (APP) through β-secretase and γ-secretase.2…”
InfluentialMalm, T., Magga, J. M., & Koıstınaho, J. (2012) · Current Translational Geriatrics and Experimental Gerontology Reports · doi:10.1007/s13670-011-0004-z · Cited by 9
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“In APP/PS1 mouse models, microglia shift toward a proinflammatory phenotype with high IL-1 β and TNF-α release [111], while LPS-stimulated primary microglia exhibit enhanced NLRP3 inflammasome activity [112].”
Topological Dissection of Proteomic Changes Linked to the Limbic Stage of Alzheimer’s Disease
Velásquez, E., Szeitz, B., Gil, J., Murillo, J. R., Palkovits, M., Renner, É., Hortobágyi, T., Döme, P., Nogueira, F. C. S., Marko‐Varga, G., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.750665 · Cited by 8
“Their results suggest that the microglia switches from an activated phenotype to an inflammatory profile at the onset of the disease (59).”
BackgroundCorrelation Analysis between External Factors and Students’ Physics Learning Achievement
Karyadi, K., Sinon, I. L. S., Yusuf, I., & Widyaningsih, S. W. (2018) · Scientiae Educatia · doi:10.24235/sc.educatia.v7i1.2415 · Cited by 9
Jang, B.-K., Shin, S. J., Park, H. H., Kumar, V., Park, Y., Kim, J. Y., Kang, H., Park, S. Y., Kwon, Y., Shin, S.-E., et al. (2024) · Pharmaceutics · doi:10.3390/pharmaceutics17010013 · Cited by 7
Anton, P. E., Twardy, S. M., Nagpal, P., Moreno, J. A., Burchill, M. A., Chatterjee, A., Busquet, N., Mesches, M. H., Kovacs, E. J., & McCullough, R. L. (2025) · Journal of Leukocyte Biology · doi:10.1093/jleuko/qiaf024 · Cited by 9
Fan, J., Ma, Z., Zheng, Y., Zhang, M., Huang, L., & Liu, H. (2023) · Nutrients · doi:10.3390/nu15163501 · Cited by 7
“A study conducted on animals suggested that M2-type microglia with the ability to phagocytose Aβ in 6 months old mice transform into M1-type phenotypes at 18 months old, which is linked to Aβ oligomer accumulation [18].”
BackgroundGardner, R. S., Kyle, M. M., Hughes, K., & Zhao, L. (2024) · Biomolecules · doi:10.3390/biom14070827 · Cited by 7
Neuroglia in neurodegeneration: Alzheimer, Parkinson, and Huntington disease
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Sanberg, P. R., Eve, D. J., & Borlongan, C. V. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1118-9_25 · Cited by 8
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Hajji, N., Calvert, C., Ritchie, C. W., & Sastre, M. (2013) · Royal Society of Chemistry eBooks · doi:10.1039/9781849735896-00080 · Cited by 7
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Pilkington, A. W., & Legleiter, J. A. (2019) · AIMS Biophysics · doi:10.3934/biophy.2019.1.1 · Cited by 7
Imaging of Microglial Activation in Alzheimer’s Disease by [11C]PBR28 PET
Donat, C. K., Mirzaei, N., Tang, S.-P., Edison, P., & Sastre, M. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-7704-8_22 · Cited by 8
Amyloid Beta, TNFα and FAIM-L; Approaching New Therapeutic Strategies for AD
Carriba, P., & Comella, J. X. (2014) · Frontiers in Neurology · doi:10.3389/fneur.2014.00276 · Cited by 7
Wang, L., Li, W., Wu, W., Liu, Q., You, M., Liu, X., Cheng, Y., Chen, J., Tan, Q., Liu, G., et al. (2024) · Brain Research · doi:10.1016/j.brainres.2024.149339 · Cited by 6
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Lopes, P. A., Pádua, M. S., & Guil‐Guerrero, J. L. (2025) · Journal of dementia and Alzheimer's disease · doi:10.3390/jdad2010002 · Cited by 9
Jiang, F., Wang, N., & Meng, Q. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251360321 · Cited by 6
“21 Dementia is also associated with impaired synaptic plasticity, APOE4 gene expression in glial cells, 22 many other CNS diseases, and damage to the BBB.”
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“M2 microglia can be generated in vitro in response to Th2 cytokines, appear to cluster around Ab plaques in AD,(35) and predominate in early preclinical stages of both AD and ALS, with a shift to M1skewed phenotypes in late disease.(29,35) Studies characterizing the inflammatory profiles of microglia in experimental p…”
ResultNeuroinflammation in Alzheimer's, Parkinson's and Huntington's Diseases
Sastre, M., Katsouri, L., Birch, A. M., Renziehausen, A., Dexter, D. T., Crichton, R. R., & Ward, R. J. (2014) · Wiley eBooks · doi:10.1002/9781118406557.ch6 · Cited by 6
Tang, J., Zhang, Y., Wang, Y., Fu, Y., Qi, J., Xiang, A., Zhao, R., Tan, G., Deng, H., Zhou, X., et al. (2025) · Journal of Inflammation Research · doi:10.2147/jir.s557031 · Cited by 5
Ardanaz, C. G., Ezkurdia, A., Bejarano, A., Echarte, B., Smerdou, C., Martišová, E., Martínez-Valbuena, I., Luquín, M. R., Ramírez, M. J., & Solas, M. (2023) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.3c00092 · Cited by 5
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Ali, W., Choe, K., Rehman, I. U., Park, H. Y., Jang, S., Ullah, S., Park, T. J., & Kim, M. O. (2025) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-025-10243-0 · Cited by 4
“Triggering of TLR4 glial cells surface receptor leads to activation of astromicroglial cells inducing apoptosis cell death, and neurodegeneration (Ali et al. 2020; Jimenez et al. 2008 ).”
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Harry, G. J., & McPherson, C. A. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_55 · Cited by 5
Yoon, S., & Kim, Y. (2015) · Global Medical Genetics · doi:10.3934/genet.2015.3.230 · Cited by 5
“Indeed, the characteristic switch from M2 to M1 seems to align with disease progression and age [45,46].”
Takeuchi, H. (2013) · Advances in Neuroimmune Biology · doi:10.3233/nib-130057 · Cited by 3
“Thus, it is suggested that whether activated microglia exert a neurotoxic or a neuroprotective effect depends on their environments including spatiotemporal changes in microglial distribution and the sort and magnitude of stimuli [53–56].”
BackgroundŞahin, S., Şahin, E., Esenülkü, G., Renda, G., Gürgen, S. G., Alver, A., Abidin, İ., & Cansu, A. (2024) · Journal of Nutrition · doi:10.1016/j.tjnut.2024.02.017 · Cited by 4
Викторович, К. В., Davydova, T. V., & Fomina, V. G. (2014) · Biology Bulletin · doi:10.1134/s1062359014020034 · Cited by 3
Functional properties of microglia in mouse models of Alzheimer’s disease
Saiepour, N. (2017) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-6117 · Cited by 3
Tang, J., Cao, Z., Lei, M., Yu, Q., Mai, Y., Xu, J., Liao, W., Ruan, Y., Shi, L., Yang, L., et al. (2024) · Archives of Gerontology and Geriatrics · doi:10.1016/j.archger.2024.105582 · Cited by 2
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Park, S. E., Cha, Y. J., Kim, Y., Kim, H. K., Kwon, C., Oh, Y. R., Kim, G., Kim, K. G.-H., Lee, H., Kang, Y. P., et al. (2026) · Neurotherapeutics · doi:10.1016/j.neurot.2026.e00851 · Cited by 3
“Additionally, microglia can form physical barriers that restrict the propagation of A β plaques [4,5].”
Development of early biomarkers of Alzheimer's disease: A precision medicine perspective
Sarkar, S., Das, N., & Sambamurti, K. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-824010-6.00006-x · Cited by 2
Biomarkers for Neurodegenerative Diseases
Abdelmoaty, M. M., Lu, E., & Foster, E. G. (2024) · Springer eBooks · doi:10.1007/978-3-031-68237-7_44 · Cited by 2
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Kitchigina, V. F., Popova, I. Y., & Shubina, L. (2025) · Neuroscience and Behavioral Physiology · doi:10.1007/s11055-025-01784-1 · Cited by 2
“The disease is caused by the release from activated microglia of substances able to affect astrocytes and having damaging effects due to their excitotoxicity and the generation of reactive oxygen species [Jimenez et al., 2008; Solas et al., 2013].”
Masilamoni, G. J., & Smith, Y. (2017) · The Receptors · doi:10.1007/978-3-319-56170-7_6 · Cited by 2
Reyes‐Resina, I., Jiménez, J., Navarro, G., & Franco, R. (2019) · BIO-PROTOCOL · doi:10.21769/bioprotoc.3385 · Cited by 2
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BackgroundSalvadores, N., Moreno‐González, I., Gamez, N., Quiroz, G., Vegas, L., Escandón, M., Jiménez, S., Vitórica, J., Gutiérrez, A., Soto, C. A., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.08.27.457960 · Cited by 2
Anton, P. E., Nagpal, P., Moreno, J. A., Burchill, M. A., Chatterjee, A., Busquet, N., Mesches, M. H., Kovacs, E. J., & McCullough, R. L. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.02.26.582114 · Cited by 2
Impact of Klotho genotype on lactylation in Alzheimer’s disease and mechanistic insights
Cai, Y., Li, L., & Li, Z. (2026) · Immunity & Ageing · doi:10.1186/s12979-026-00563-x · Cited by 1
Trem2 Variants and Alzheimer‘s Disease
Tosto, G., & Reitz, C. (2013) · Future Neurology · doi:10.2217/fnl.13.22 · Cited by 1
Jiang, R., Chi, X.-D., Jing, Y., Wang, B., & Li, S. (2023) · Aging · doi:10.18632/aging.204605 · Cited by 1
Jin, M., Xu, R., Wang, L., Alam, M. M., Ma, Z., Zhu, S., Martini, A. C., Jadali, A., Bernabucci, M., Xie, P., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.12.22.473858 · Cited by 1
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Sharma, S., Borski, C., Hanson, J. L., Garcia, M. A., Link, C. D., Hoeffer, C. A., Chatterjee, A., & Nagpal, P. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.08.23.505002 · Cited by 1
Targeting Early Stages of Alzheimer’s Disease in a Transgenic Model
Lord, A. (2009) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
Characterization of the Role of Nicotine and Delta 9-THC in Modulation of Neuroinflammation
Ehrhart, J. C. (2010) · Digital Commons - University of South Florida (University of South Florida)
Ageing and the Immune Response in the CNS
Raj, D. D. A., Eggen, B. J. L., & Boddeke, H. W. G. M. (2014) · Wiley eBooks · doi:10.1002/9781118406557.ch4
Darlington, D. (2014) · Digital Commons - University of South Florida (University of South Florida)
Using TUDCA to treat Alzheimer's disease after pathology onset in APP/PS1 mice
Dionísio, P. (2014) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT)
Review Article Microglia and ischemic stroke: a double-edged sword
Patel, A. R., Ritzel, R. M., McCullough, L. D., & Liu, F. (2013)
Using TUDCA to treat Alzheimer's disease after pathology onset in APP/PS1 mice
Farmácia, F. D. (2014)
Lynch, M. A., & Minogue, A. M. (2014) · Arrow@dit (Dublin Institute of Technology)
Activation of survival pathways triggered by death receptors in the nervous system
Fernández, F. M. (2013) · TDX (Tesis Doctorals en Xarxa)
Inflammatory pathology in neurodegenerative dementias
Niedermayer, G. (2014)
The Propagation of Neurodegenerative Diseases by Inflammation and Exosomes
Sackmann, V. (2019) · Linköping University medical dissertations · doi:10.3384/diss.diva-160949 · Cited by 1
“inflammatory phenotype around Aβ plaques during the first 6 months, when Aβ load is relatively low, but switch into a pro-inflammatory phenotype at 18 months of age, coincident with accumulated levels of Aβ [64].”
BackgroundInfluentialMalm, T., Magga, J. M., & Koıstınaho, J. (2012) · Current Translational Geriatrics and Experimental Gerontology Reports · doi:10.1007/s13670-012-0008-3
Ardanaz, C. G., Bejarano, A., Echarte, B., Smerdou, C., Martišová, E., Martínez-Valbuena, I., Luquín, M. R., Ramírez, M. J., & Solas, M. (2022) · Research Square · doi:10.21203/rs.3.rs-1381483/v1
Ardanaz, C. G., Bejarano, A., Echarte, B., Smerdou, C., Martišová, E., Martínez-Valbuena, I., Luquín, M. R., Ramírez, M. J., & Solas, M. (2022) · Research Square · doi:10.21203/rs.3.rs-1381483/v2
ALZHEİMER HASTALIĞINDA KOMPLEMAN SİSTEMİN ROLÜ
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Գալստյան, Ս. Ա. (2024) · MEDICINE SCIENCE AND EDUCATION · doi:10.56936/18291775-2024.38-7
Siedlecki‐Wullich, D., Ayral, A., Iohan, L. D. C. C., Lemeu, C., Buiche, V., Blary, K., Chapuis, J., Eysert, F., Beury, D., Delacre, M., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.08.19.671013
“This observation aligns with previous in vivo studies reporting heightened microglial reactivity in APP mice [42,43], and demonstrates that our in vitro platform can capture genotype-specific immune responses using adult microglia.”
Mullins, C. A., Gannaban, R. B., Kramer, A., Shah, H., Haque, Z. F., Ramezan, M., Dehghani, F., Palaniyappan, A., Bowers, F., MohanKumar, S. M., et al. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251389236 · Cited by 1
“43 It is noteworthy to mention that the expression of pathology or neuronal health markers can vary substantially across the age and brain regions even within the same AD mouse model.”
Li, W., Fu, H., Youdim, M. B. H., Pang, Y., & Han, Y. (2010) · Springer eBooks · doi:10.1007/978-90-481-8553-5_7
“Importantly, the concomitant injection of the anti-Aβ antibody 6E10 with Aβ oligomers neutralizes the oligomer-induced LTP dysfunction [ 53 ].”
BackgroundLaversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Figshare · doi:10.6084/m9.figshare.13278564
Han, H., Zhao, Y., Du, J., Wang, S., Yang, X., Li, W., Song, J., Zhang, S., Zhang, Z., Tan, Y., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26641543
Han, H., Zhao, Y., Du, J., Wang, S., Yang, X., Li, W., Song, J., Zhang, S., Zhang, Z., Tan, Y., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26641546
Laversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Figshare · doi:10.6084/m9.figshare.13278558
Laversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Figshare · doi:10.6084/m9.figshare.13278567
Laversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Figshare · doi:10.6084/m9.figshare.13278561
Han, H., Zhao, Y., Du, J., Wang, S., Yang, X., Li, W., Song, J., Zhang, S., Zhang, Z., Tan, Y., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26641552
Koh, S.-H., Kwon, H. S., Choi, S. H., Jeong, J. H., Na, H. R., Lee, C. N., Yang, Y., Lee, A. Y., Lee, J.-H., Park, K. W., et al. (2021) · Figshare · doi:10.6084/m9.figshare.14329456
Koh, S.-H., Kwon, H. S., Choi, S. H., Jeong, J. H., Na, H. R., Lee, C. N., Yang, Y., Lee, A. Y., Lee, J.-H., Park, K. W., et al. (2021) · Figshare · doi:10.6084/m9.figshare.14329453
Laversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Figshare · doi:10.6084/m9.figshare.13278573
Han, H., Zhao, Y., Du, J., Wang, S., Yang, X., Li, W., Song, J., Zhang, S., Zhang, Z., Tan, Y., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26641549
Laversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Figshare · doi:10.6084/m9.figshare.13278555
Siedlecki‐Wullich, D., Ayral, A., Iohan, L. D. C. C., Lemeu, C., Buiche, V., Blary, K., Chapuis, J., Eysert, F., Beury, D., Delacre, M., et al. (2026) · Journal of Neuroinflammation · doi:10.1186/s12974-026-03748-9 · Cited by 1
“This observation aligns with previous in vivo studies reporting heightened microglial reactivity in APP mice [42, 43], and demonstrates that our in vitro platform can capture genotype-specific immune responses using adult microglia.”
dos Santos, J. M. M., de Moura, A. B., Medeiros, E. B., Generoso, C. M., Tietbohl, L. T. W., Lídio, A. V., Steiner, B. T., Scussel, R., Dal‐Bó, A. G., Budni, J., et al. (2026) · Neuropeptides · doi:10.1016/j.npep.2026.102609
Fan, T., Wei, C., Chen, W., Li, S., Wang, J., Lu, Y., & Renshi, X. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1915475
“On the other hand, microglia also release inflammation factors, the roles of these inflammatory factors may lead to the neuronal death and neurodegeneration (Jimenez et al., 2008).”
Skóra, B., & Szychowski, K. A. (2026) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2026.10.045
Age, inflammation and Abeta itself influence Abeta degradation in Alzheimer's Disease
van Rijn, J. M. (2014) · Utrecht University Repository (Utrecht University)
Metadata
- Authors
- Jimenez, S., Baglietto-Vargas, D., Caballero, C., Moreno-Gonzalez, I., Torres, M., Sanchez-Varo, R., Ruano, D., Vizuete, M., Gutierrez, A., & Vitorica, J.
- Affiliations
- Universidad de Sevilla (ES)
- Universidad de Málaga (ES)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-11-05
- Volume
- 28
- Issue
- 45
- Pages
- 11650-11661
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6671312
- OpenAlex
- W2001334299
- Cited by
- 383
- References
- 70
- Citations by year
- 2026: 7 · 2025: 19 · 2024: 19 · 2023: 14 · 2022: 19 · 2021: 30 · 2020: 22 · 2019: 21 · 2018: 19 · 2017: 20 · 2016: 19 · 2015: 26 · 2014: 28 · 2013: 37 · 2012: 25
- FWCI
- 12.75
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, cc-by-nc-nd)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, other-oa)
- Repositorio Institucional de la Universidad de Málaga (University of Málaga) (submittedVersion, cc-by)
- Funders
- Ministerio de Economía y Competitividad
- Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas
- Instituto de Salud Carlos III
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, microglial activation, alternative activation, hippocampus, amyloid-beta oligomers, soluble amyloid-beta, TNF-α, neurodegeneration, age-dependent disease progression, 6E10 antibody
- MeSH terms
- Aging, Alzheimer Disease, Analysis of Variance, Animals, Disease Models, Animal, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Inflammation, Mice, Transgenic, Mutation, Phenotype, Tumor Necrosis Factor-alpha, Amyloid beta-Protein Precursor, CD3 Complex, Microglia, Lectins, CD11b Antigen, Mice, Nitric Oxide Synthase Type II, Presenilin-1
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